Significance of persistent inflammation in respiratory disorders induced by nanoparticles

Our plain-English summary of Significance of persistent inflammation in respiratory disorders induced by nanoparticles, by Y. Morimoto, H. Izumi, E. Kuroda (Journal of Immunology Research, 2014).

The study

• Authors: Y. Morimoto, H. Izumi, E. Kuroda
• Journal: Journal of Immunology Research
• Published: 2014;2014:962871
• Type of article: Review
• Cited by: 22 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Pulmonary inflammation, especially persistent inflammation, has been found to play a key role in respiratory disorders induced by nanoparticles in animal models. In inhalation studies and instillation studies of nanomaterials, persistent inflammation is composed of neutrophils and alveolar macrophages, and its pathogenesis is related to chemokines such as the cytokine-induced neutrophil chemoattractant (CINC) family and macrophage inflammatory protein-1α and oxidant stress-related genes such as heme oxygenase-1 (HO-1). DNA damages occur chemically or physically by nanomaterials. Chemical and physical damage are associated with point mutation by free radicals and double strand brake, respectively. The failure of DNA repair and accumulation of mutations might occur when inflammation is prolonged, and finally normal cells could become malignant. These free radicals can not only damage cells but also induce signaling molecules containing immunoreaction. Nanoparticles and asbestos also induce the production of free radicals. In allergic responses, nanoparticles act as Th2 adjuvants to activate Th2 immune responses such as activation of eosinophil and induction of IgE. Taken together, the presence of persistent inflammation may contribute to the pathogenesis of a variety of diseases induced by nanomaterials.

In plain English

This article was a review, not a new study. The authors discussed published animal and cell studies, including some of their own, on how persistent lung inflammation may be involved in lung disorders caused by nanoparticles such as nickel oxide, titanium dioxide and carbon nanotubes. Asbestos was also reviewed because multiwalled carbon nanotubes had been reported to be similar to asbestos. The studies described included a rat experiment in which 20 days of chrysotile inhalation was followed by continuing inflammation and fibrosis. They also described the authors' earlier rat study, in which crocidolite asbestos or crystalline silica placed in the lungs caused inflammation lasting until 6 months later, while micron-sized titanium dioxide caused only short-lived inflammation. The authors explained how free radicals, which asbestos and nanomaterials can produce, may damage DNA. They noted studies with differing findings on whether asbestos exposure is linked to K-ras gene mutations, and discussed particles boosting allergic responses. The authors concluded that persistent inflammation may contribute to diseases caused by nanomaterials. They said further research is needed to determine whether persistent inflammation causes cancer.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Narrative review of published animal, cell and some human studies, including the authors' own earlier work; no review methods (search strategy, selection criteria) are described
• Who was studied: Published inhalation and intratracheal instillation studies, mainly in rats and mice, plus cell studies and some studies of human lung tumors; the number of studies reviewed is not stated
• Exposure: Nanomaterials (nickel oxide nanoparticles, titanium dioxide, fullerene, carbon nanotubes and nanofibers), with asbestos (chrysotile, crocidolite) and crystalline silica discussed for comparison
• Main results:
  • In a reviewed study in rats, 20 days of chrysotile inhalation was followed by continuous inflammation and fibrosis containing mainly neutrophils (a type of white blood cell)
  • In the authors' earlier rat study of mineral fibers placed in the lungs (intratracheal instillation), crocidolite asbestos or crystalline silica caused persistent inflammation from the start until 6 months later, while micron-sized titanium dioxide caused only transient early inflammation
  • In a reviewed rat study, nickel oxide nanoparticles caused persistent neutrophil inflammation in the lung from 3 days to 3 months after intratracheal instillation
  • The authors stated that free radicals are produced on the surface of asbestos and nanomaterials by inflammatory or lining cells that take them up, and that this can lead to DNA damage
  • Reviewed studies on asbestos and K-ras gene mutations differed: one reported that asbestos exposure increases mutation at K-ras codon 12, while another reported that asbestos exposure alone was not significantly associated with more K-ras mutations, but found a strong association between adenocarcinoma and K-ras mutation in smokers with asbestos exposure
  • A reviewed study reported that single-wall carbon nanotubes and carbon nanofibers, but not asbestos, increased K-ras mutations in the lung
  • The authors described an immune sensor in cells (the NLRP3 inflammasome) as being activated by particles including aluminum salts, crystalline silica and asbestos
• The authors' conclusion: The authors concluded that persistent inflammation may contribute to diseases caused by nanomaterials, and that further research is needed to determine whether persistent inflammation causes cancer
• Limitations the authors state:
  • The authors stated that the effect of nanomaterials on the human body is inconclusive
  • The authors stated that there are few reports on nanoparticles and oncogene mutation
  • The authors stated that the best dose of nanoparticles for testing harmful effects in animals is not known, and that excess doses can cause artificial effects
  • The authors stated that how particles act in immune responses is poorly understood

Topics

Medical terms in this study, explained in our Lexicon: Inflammation, Alveolar Macrophage, Cytokine, Macrophage, Damages.

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